ABSTRACT
OBJECTIVES: This study was aimed to explore the effects of follistatin on cisplatin-induced renal dysfunction, histopathological changes, apoptosis, inflammation and oxidative damage in rats. BACKGROUND: Follistatin plays an important role in the developmental and regeneration processes of kidney by blocking the actions of activin, which is a member of transforming growth factor-ß superfamily. METHODS: Twenty seven rats were separated into 4 equal groups: Control, Cp (cisplatin, 6 mg/kg, intrapertoneally (ip)), F1 (cisplatin + 1 µg/day follistatin ip for 4 consecutive days) and F4 (cisplatin + 4 µg/day follistatin ip single dose) groups. Renal health was monitored by blood urea nitrogen, serum creatinine and histological analysis. Apoptosis, inflammation and oxidative stress was investigated in kidney tissue. Activin A levels in serum and kidney were evaluated as well. RESULTS: Follistatin administration showed a considerable nephroprotective effect against cisplatin-induced nephrotoxicity by preventing renal functional and structural abnormalities, apoptosis and inflammation. The activin A levels in both serum and kidney were also suppressed by follistatin administration. CONCLUSION: Exogenous follistatin ameliorates acute kidney injury, by blocking activin A. The renoprotective effect of follistatin against cisplatin-induced nephrotoxicity appears to be associated with its anti-inflammatory, antiapoptotic and direct nephroprotective actions (Tab. 1, Fig. 7, Ref. 23).
Subject(s)
Acute Kidney Injury , Cisplatin , Follistatin , Acute Kidney Injury/chemically induced , Acute Kidney Injury/drug therapy , Animals , Apoptosis/drug effects , Cisplatin/adverse effects , Follistatin/pharmacology , Follistatin/therapeutic use , Inflammation , Kidney , Oxidative Stress , RatsABSTRACT
There is clinical proof of the decisive therapeutic effect of bolus injection of corticosteroids in septic shock. Our own studies, in which sublethal doses of bacterial suspensions were introduced into the peritoneal cavity of guinea pigs, demonstrate that a simultaneously applied solution of methylprednisolone (MP) has no influence on the intraperitoneal number of bacteria. Even the rapid initial decrease of bacterial counts, which, according to our studies, can be inhibited by Liquoid and is, therefore, caused by complement, is not influenced by the addition of MP. There was no indication of a change of tissue reactions in gut or mesenterium. The therapeutic effect of corticosteroids seems to depend on its influence on peripheral vessels.
Subject(s)
Bacterial Infections/drug therapy , Methylprednisolone/therapeutic use , Peritonitis/drug therapy , Animals , Ascitic Fluid/microbiology , Escherichia coli Infections/drug therapy , Guinea Pigs , Peritonitis/pathologyABSTRACT
The lunate bone receives its blood-supply via a palmar and a dorsal vascular and fibrous strand. When the wrist is extended the dorsal vessels are caught in a kind of vice formed by the radius and the capitate bone and compressed up to complete occlusion. This mechanism, important for the pathogenesis of Kienböck's disease, is demonstrated on anatomical specimens.
